• Title, Summary, Keyword: nitric oxide

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Taurine Activates ERK2 and Induces the Production of Nitric Oxide in Osteoblast-like UMR-106 Cells

  • Park, Sung-Youn;Kim, Harriet;Kim, Sung-Jin
    • Proceedings of the Korean Society of Applied Pharmacology
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    • pp.145-145
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    • 1998
  • In the present study, we have demonstrated that taurine could stimulate the production of nitric oxide and the activity of ERK2 (extracellular signal regulated protein kinase or pp42 MAP kinase). Nitric oxide(NO), the product of inducible nitric oxide synthase(iNOS), is known to be implicated in the metabolism of bone. ERK cascade plays a key role in the gene expression of iNOS in osteoblastic cell. We investigated whether taurine (l-20mM) could stimulate ERK2 activity, nitric oxide production, and inducible nitric oxide synthase in osteoblast-like UMR-106 cells. Nitric oxide was measured spectophotometrically as nitrite and the activation of ERK2 and iNOS was studied using Western 145 blot analysis. Taurine increased the production of nitric oxide in a dose-dependent manner and the effect was reached to a maximum at 10 mM. The activation of iNOS were consistent with NO levels. The tyrosine phosphorylation of ERK2 was increased by taurine in a time-dependent manner. The these result suggest that taurine might stimulate the production of nitric oxide in osteoblast-like cells by the activation of ERK2 and could regulate the metabolism of bone via nitric oxide.

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The Role of Nitric Oxide in Menadione-Induced Cytotoxicity in Rat Platelets (Menadione에 의한 흰쥐 혈소판 세포독성에서 nitric oxide의 역할)

  • 승상애;김대병;윤여표;정진호
    • Toxicological Research
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    • v.11 no.2
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    • pp.303-308
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    • 1995
  • Nitric oxide, a physiological transmitter, is reported to mediate cellular injury in various tissues. Its reactivity to free radical is believed to be one of the reasons for its involvement in cytotoxicity. Menadione, a representative quinone, is cytotoxic to several cell systems including isolated hepatocyte, endothelial cell and red blood cells. Its toxic mechanism is related to oxidative stress, mediated by toxic free radicals. Our previous studies demonstrated that menadione induced cell lysis and increase of oxygen consumption in platelets. It has been reported that platelets have nitric oxide producing enzyme, nitric oxide synthase. Thus, we have investigated to manifest the role of nitric oxide.in menadione-induced cytotoxicity in rat platelets. Menadione induced cytotoxicity in platelets was unaffected by $N^G$-nitro-arginine methyl ester (L-NAME), selective and competitive inhibitor of nitric oxide synthase. We also invesitgated the role of extracellular nitric oxide in menadione-induced cytotoxicity of platelets by addition with sodium nitroprusside (SNP). SNP did not affect platelet cytotoxicity by menadione. These results suggested that nitric oxide which was generated endogeneously or exogeneously might have a negligible role in menadione-induced cytotoxicity in rat platelets.

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Change of the Radiation-induced NO(nitric oxide) in Mice with Treatment by Algin-oligosaccharide (알긴산올리고당 처치 마우스에서 방사선 유도 산화질소의 변화)

  • Jang, Woo-Young;Choi, Seong-Kwan;Dong, Kyung-Rae
    • The Journal of the Korea Contents Association
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    • v.9 no.7
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    • pp.211-217
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    • 2009
  • In order to find out the radioprotective effect of algin-oligosaccharide, this study, with a mouse of which whole body irradiated by 3 Gy radiation once, measured nitric oxide. In nitric oxide test for observing the reaction of cell inflammation, nitric oxide showed decreased in the irradiation control group, while 3 day's treatment group with algin-oligosaccharide before or after irradiation indicated higher than the irradiation control group, especially showed big difference in 3 day's treatment group before irradiation (P<0.001). Consequently, this study inquired into the fact that algin-oligosaccharide with superior antioxidant activity performed radiation protection by increasing promotion of nitric oxide generation and confirmed that natural product with less chemical toxicity was able to be applied as radioprotector.

The Relationship Between Firing Modes and Nitric Oxide Emission In Highly Preheated Air Combustion

  • Choi, Gyung-Min;Katsuki, Masahi;Kim, Duck-Jool
    • Journal of Mechanical Science and Technology
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    • v.14 no.4
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    • pp.433-440
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    • 2000
  • The influence of combustion air at temperatures on nitric oxide emission was studied. The nitric oxide emission generally increases with a rise in the temperature of the combustion air. However, if combustion products for dilution of fuel or combustion air are used before the combustion reaction, then the nitric oxide emission can be reduced even when highly preheated air for combustion air is used. Combustion in low oxygen concentrations flattens the firing mode, resulting in a uniform reaction, and, thus, low nitric oxide emission can be achieved.

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Role of Exogenous Nitric Oxide Generated through Microwave Plasma Activate the Oxidative Signaling Components in Differentiation of Myoblast cells into Myotube

  • Kumar, Naresh;Shaw, Priyanka;Attri, Pankaj;Uhm, Han Sup;Choi, Eun Ha
    • Proceedings of the Korean Vacuum Society Conference
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    • pp.158-158
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    • 2015
  • Myoblast are myogenic precursors that proliferate, activate, and differentiate on muscle injury to sustain the regenerative capacity of skeletal muscle; The neuronal isoform of nitric oxide synthase (nNOS, termed also NOS-I) is expressed in normal adult skeletal muscle, suggesting important functions for Nitric oxide (NO) in muscle biology1,2,3. However, the expression and subcellular localization of NO in muscle development and myoblast differentiation are largely unknown. In this study, we examined effects of the nitric oxide generated by a microwave plasma torch, on proliferation/differentiation of rat myoblastic L6 cells. Experimental data pertaining to nitric oxide production are presented in terms of the oxygen input in units of cubic centimetres per minute. The various levels of nitric oxide are observed depending on the flow rate of nitrogen gas, the ratio of oxygen gas, and the microwave power4. In order to evaluate the potential of nitric oxide as an activator of cell differentiation, we applied nitric oxide generated from the microwave plasma torch to L6 skeletal muscles. Differentiation of L6 cells into myotubes was significantly enhanced the differentiation after nitric oxide treatment. Nitric oxide treatment also increase the expression of myogenesis marker proteins and mRNA level, such as myogenin and myosin heavy chain (MHC), as well as cyclic guanosine monophosphate (cGMP), However during the myotube differentiation we found that NO activate oxidative stress signaling erks expression. Therefore, these results establish a role of NO and cGMP in regulating myoblast differentiation and elucidate their mechanism of action, providing a direct link with oxidative stress signalling, which is a key player in myogenesis. Based on these findings, nitric oxide generated by plasma can be used as a possible activator of cell differentiation and tissue regeneration.

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Ginsenoside Rg1 Stimulates Nitric Oxide Release in Pulmonary Artery Endothelial Cells in Culture

  • Kim, Hye-Young
    • BMB Reports
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    • v.28 no.4
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    • pp.301-305
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    • 1995
  • Considering the stimulatory effects of ginsenosides from Panax ginseng C. A. Meyer on the release of nitric oxide from bovine aortic endothelial cells in vitro and vasodilatation of rabbit pulmonary artery in vivo, the present study is designed to investigate the mechanism of nitric oxide release by ginsenosides in calf pulmonary artery endothelial cells, Nitric oxide release was determined in endothelial cells treated with ginsenosides and compared with those of the receptor-dependent agonists, bradykinin and ADP and the receptor-independent calcium ionophore $A_{23187}$. The results showed that total saponin and ginsenoside $Rg_1$, not $Rb_1$, stimulated nitric oxide release measured as conversion to L-citrulline. The nitric oxide releasing properties of total saponin and ginsenoside $Rg_1$ were different; total saponin stimulated only conversion to L-citrulline, like $A_{23187}$, while ginsenoside $Rg_1$ stimulated both L-arginine transport and conversion to L-citrulline, as bradykinin or ADP did.

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Inhibition of Nitric Oxide Synthesis by 8-epi-xanthatin in Activated RAW 264.7 Cells (활성화한 RAW 264.7 세포주에서 8-epi-xanthatin의 Nitric Oxide 생성저해)

  • Lee, Hwa-Jin;Jeong, Yeon-Su;Ryu, Shi-Yong;Ryu, Jae-Ha
    • YAKHAK HOEJI
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    • v.42 no.5
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    • pp.540-543
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    • 1998
  • The nitric oxide (NO) produced in large amounts by inducible nitric oxide synthase is known to be responsible for the vasodilation and hypotension observed in septic shock. We have found that 8-epi-xanthatin from Xanthium strumarium L. inhibited the production of NO in LPS-activated RAW 264.7 cells ($IC_{50}$ value was 1.5 ${\mu}$M). This activity was resulted from the suppressing of inducible nitric oxide synthase enzyme expression.

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Influence of the Cyclic Parameters on the Nitric Oxide Formation in the diesel Engine

  • Rosli Abu Bakar
    • Transactions of the Korean Society of Automotive Engineers
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    • v.6 no.1
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    • pp.27-35
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    • 1998
  • This study describes the influence of combustion parameters on the nitric oxide emission, such as injection timing, air flow rate, injected amount of fuel, and compression ratio of engine. In order to determine the influence factors on the nitric oxide emission, the experiment were investigated with various parameters of engine cycle. According to the results of this study, the retardation of injection timing and the increases of airflow rate, and the decreases of fuel injection amount reduce the nitric oxide concentration in the exhaust emissions. Also, the increases of compression ration of engine increase in the concentration of nitric oxide formation in the combustion chamber. The results of this study give a guideline to decrease the nitric oxide formation by using the simulation program.

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Immunohistochemical Changes of Apoptotic Control Genes by Chronic Inhibition of Nitric Oxide in Rats

  • Bae, Hyung-Joon
    • Biomedical Science Letters
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    • v.18 no.4
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    • pp.420-427
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    • 2012
  • Sprague-Dawley (SD) rats were orally administered with NG-nitro-L-arginine methyl ester (L-NAME), which inhibits or blocks the production of nitric oxide from L-arginine in vascular endothelial cells and vessel tissue. We examined the effects of nitric oxide on some physiological changes such as blood pressure and heart rate, and confirms the apoptosis induced by the suppressed nitric oxide activity in the kidney. This study was performed to investigate correlation between the activities of nitric oxide and apoptosis by immunohistochemical changes of apoptotic control proteins with regulated chronic inhibition of nitric oxide. In the kidney from L-NAME-treated group, immunohistochemical reaction to the antigens of apoptosis inhibiting proteins such as bcl-2 and bcl-xL, exhibited a time-dependent reduction. The expression of apoptosis-inhibiting proteins such as bax and p53 increased expression in proportion to the duration of treatment. The most sensitive apoptosis regulating proteins to L-NAME were p53 in stimulation and bcl-2 in inhibition, respectively.

Inhibition of TCDD Induced Cyplal Expression by SNP In Hepa I Cells

  • Kim, Ji-E.;Sheen, Yhun-Y.
    • Biomolecules & Therapeutics
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    • v.7 no.4
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    • pp.315-321
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    • 1999
  • Since it has been known that hypoxia increases inducible nitric oxide synthase (iNOS) gene expression through hypoxia responsive element, it was possible to establish the hypothesis that nitric oxide could be a mediator of hypoxia to inhibit Cyplal promoter activity. In order to test this hypothesis, we have undertaken the study to examine the effects of hypoxia and nitric oxide on Cyplal promoter activity in Hepa I cells. Mouse Cyplal 5'flanking DNA, 1.6 Kb was cloned into pGL3 expression vector in order to construct pmCyplal-Luc. Hepa I cells were transfected with pmCyplal-Luc and were treated with $10^{-9}$ M TCDD and nitric oxide producing agents, such as lipopolysaccharide(LPS), sodium nitroprusside (SNP). Luciferase activity of reporter gene was measured from pmCyplal-Luc transfected Hepa I cell lysate which contains 2 g total protein using luciferin as a substrate. Nitric oxide producing agents, such as lipopolysaccharide (LPS), sodium nitroprusside(SNP) showed inhibition of luciferase activity that was induced by $10^{-9}$M TCDD treatment with dose dependent manner. Concomitant treatment of 1mM $N^G$-nitro-ι-arginine with $10^{-6}$~$10^{-4}$M sodium nitro-prusside recovered luciferase activity from the TCDD induced luciferase activity that was inhibited by nitric oxide producing agents. These demonstrated that nitric oxide could be a mediator of inhibitors on dioxin induced Cyplal expression in Hepa I cells.

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